Phytopathology
Plants like all organisms can become diseased. They grow old, they are attacked by parasitic fungi, insects, bacterial and viral infections. In addition to these factors, they also can be affected by the alleopathic effects of other plants, disruption of root space and changes in the water table.
Most plant diseases have either cures or controls. Controls being the prefered option. Diseases can be prevented before they occur, by numerous methods. These measures may be time consuming and expensive. Therefore, for ornamental plants, people generally prefer to attempt a cure after diseases become manifest. Not all diseases are so easy to treat. Consider chestnut blight.
Mountain Pine Beetle
The mountain pine beetle, Rocky Mountain beetle, or Black Hills beetle (Dendroctonus ponderosae), is a small beetle, less than 5 mm long, that bores into the bark of pine trees. There it lays its eggs, the hatching larvae feed in the bark, i.e. the phloem, of pine trees. It over-winters as a larva in the bark. In the northern States and Canada, the beetle usually has but one complete generation per year. The beetle infests mostly the lodgepole, limber and ponderosa pines. Western white pine, Scots pine, and other Pinus species can be affected also. Mostly these beetle infestations occur in the far west, and it is stands of lodgepole and ponderosa pine that are most often decimated. It can live in jack pine. By the 1990s it was known to occur in jack-lodgepole pine hybrids - in the eastern Rockies. Indeed, by the early 2010s the beetle was detected in pure-strain jack pines.
Outbreaks tend to be localised, but large in overall extent. It is not usually the mountain pine beetle itself that kills a pine tree. It is rather a series of ‘blue stain’ fungi that do this injury (eg. Ophiostoma clavigerum & Ophiostoma montium). These fungi start in the phloem, but the mycelia can eventually spread into the sapwood. If they grow too prolifically they can block the tree’s sap-flow - thereby killing the tree. As is often the case, various kinds of fungi live symbiotically with the beetle. The beetle larva eats the fungal mycelium of these fungi, and the adult spreads the fungal spores. But not all kinds of fungi are eaten by the beetle larva. The “green stain” fungi are eaten by the bark beetles, but they are not a primary foodstuff. Indeed the green stain fungi seem mostly to use the beetle as a vector. Besides which, the fungi are as much carried by parasitic mites as by the bark beetle itself. Though there is some evidence that the green stain fungi weaken the pine tree host, and thereby benefit the beetle.
Mountain pine beetle is native to western North America. However, pine die-off has reached ‘pandemic’ (panphytic?) proportions in the last decade. Vast swaths of pine forest have been killed so far by the beetle-fungus combo. It seems that global warming may have decreased the winter mortality of the beetle. With more beetles surviving winter, woodpeckers and other natural controls cannot always keep up. Outbreaks may also be exacerbated by the shorter dormant season for which the pines are perhaps somewhat maladapted. The beetle and its fungi mostly afflict old trees, dought stressed trees and/or over-crowded stands. There is some evidence that the pine beetle populations tend to flare up in even-aged stands. This is because it is mostly mature trees that are suitable nurseries for the beetle. Indeed some of the largest beetle outbreaks have occurred in so-called “managed” forests. Hence the forestry practices of clear-cutting and mass replanting have not always been helpful. Massive stands of prime beetle habitat mean huge beetle population booms are possible. Unfortunately this means that massive swarms of beetles can form. Once these swarms occur, even mixed-age stands downwind can succumb to the beetles.
Systemic insecticides can control the beetle. Controlled burning of moribund trees does work. Sometimes burning is the only workable option. Diligence is needed to slow the beetle's eastward trek.
References
Adams, Aaron S. & Six, Diana L., 2007. Temporal variation in mycophagy and prevalence of fungi associated with developmental stages of Dendroctonus ponderosae (Coleoptera: Curculionidae). Environmental Entomology. 36 (1): 64-72.
Kerr, Pat. 2011. Mountain Pine beetle jumps tree species. Tree Service Canada. 5 (1): 1 & 4.
Kim, J-J.; Kim, S.H. Lee, S. and Breuil, C. 2008. Distinguishing Ophiostoma ips and Ophiostoma montium, two bark beetle-associated sapstain fungi. FEMS Microbiology Letters 222: 187-192.
Rice, A.V and Langor, D.W. 2009. Mountain pine beetle-associated blue-stain fungi in lodgepole · jack pine hybrids near Grande Prairie, Alberta (Canada). For. Path. 39: 323–334.
Six, D.L. and Klepzig, K.D. 2004. Review article. Dendroctonus Bark Beetles as Model Systems for Studies on Symbiosis. Symbiosis, 37 (1-3): 1-26.
Solheim, Halvor and Krokene, Paal. 1998. Growth and virulence of mountain pine beetle associated blue-stain fungi, Ophiostoma clavigerum and Ophiostoma montium. Canadian Journal of Botany. 76(4): 561–566.
Beech Bark Disease
In the 1890s a European scale insect (Cryptococcus fagisuga) was accidently introduced to North America. The scale insect feeds on the phloem-sap of beech trees (Fagus spp.). It mostly feeds in tiny crevasses of the otherwise smooth beech bark. It is a rather typical scale insect. It is pale and about 0.5 to 1 mm long, the adult bug is housed in a waxy shell or 'scale'.
Unfortunately the holes bored by this foreign bug proved to be portals for the fungus Nectria coccinea var. faginata, and sometimes also Nectria galligena fungus. The nectria fungus has orange bead-like sexual fruiting bodies. The asexual fruiting bodies are pale. These bodies tend to cluster in cracks in the bark - cracks that they cause. The mycelium feeding in the bark can kill sections of the phloem (bark). Near the points of infection very persistent cankers can form. These cankers can eventually girdle and kill the beech tree. The American beech (F. grandifolia) seems to be more sensitive to the disease-combo than does the European species (F. sylvatica).
The combination of the insect and fungus proved to be dire, it causes beech bark disease, which is sometime fatal. Luckily the disease spread slowly starting on the East Coast. By 2009 the disease had crossed the Great Lakes and St. Lawrence into Quebec and Ontario. It is difficult to control either the scale insect or the fungus. One can, however, attempt to halt the westward spread of the disease. One means would be to limit the transport and planting of European beech trees in Ontario. It is advisable therefore not to transplant beech trees or use them as ornamentals.
Chestnut Blight
American Sweet Chestnuts (Castanea dentata) are trees in the beech-oak family. Sweet chestnuts were once common in the Carolinian deciduous forests of eastern North America. In some forests associations they were the dominant species, often a quarter or more of the trees per stand were sweet chestnuts. Sweet chestnuts were most often associates with black oak, white oak, shagbark hickory, white ash and black cherry.
There are other species of chestnut. The European Castanea sativa, and the Asian Castanea mollissima, are similar and produce edible seeds. These species are, however, less damaged by chestnut blight than their American relative.
In 1904 a fungal disease (Cryphonectria parasitica) of Asian origin was introduced, by accident, to New York State. The fungus growing in the thin sapwood of the sweet chestnuts encountered insufficient resistance from the trees' defences. By 1925 this fungus infestation spread to almost the whole of the sweet chestnut's native range. Eventually, almost every sweet chestnut stand was infected. Isolated trees, and some coppice sprouts, are still producing seeds. The coppice sprouts are not good at re-establishing roots. And the old stumps are being slowly rotted away by the chestnut-tongue fungus (Fistulina hepatica). However, a few adult trees still exist. This author has seen blight-free chestnuts near the coast of Lake Erie. Perhaps they are there protected from blight spores by the direction of the wind. All hope is not lost.
Cryphonectria parasitica is a canker fungus. It causes lesions on branches or stems. On other tree species, such as oaks and hickories, the fungus seems to be purely saprophytic, meaning that it feeds on wood that is already dead. To the genus Castanea, however, the fungus is truly parasitic, it manages to kill living wood, and then it digests the now-dead tissue. It is an ascomycete fungus and produces ascospores, sexually produced spores. Ascospores are released from a small disc-like 'perithecia' bodies that develop on the bark. These ascospores are generally wind-dispersed. This fungus also produces conidia, which are asexual spores. These conidia are present in a sticky orange tendrils that ooze from the conidiospore producing bodies called 'pycnidia'. Conidia are most often spread by insects, birds and other mobile vectors that come in contact with the sticky ooze.
Like many ascomycete species, the blight also has deuteromycete forms. Some strains of the chestnut blight do not seem to produce ascospores, only conidiospores. These asexual anamorphs are known as Endothiella parasitica.
Control
Several scientists are still trying to breed blight resistant strains of chestnut. For, unfortunately, there appears to be no effective post-infection treatment for chestnut blight. So far, there has been little sign of progress.
A similar fate has fallen on the butternut, the white elm, and the ash trees. All of trees are threatened by fungal diseases which have been spread by human agency. Likewise, several European and Asian plants have been infected by fungi of American origin. If there is any object lesson in this, it is to be careful with introducing organisms to places where they are not native. Often this mixus cannot be avoided.
References
Eastman, John. 1992. The Book of Forest and Thicket. Stackpole Books. Mechanicsburg, PA.
Holliday, Paul. 1989. A Dictionary of Plant Pathology. Cambridge University Press. Cambridge.
Dutch Elm Disease
Dutch elm disease, or 'elm wilt', is more famous, now, than chestnut blight, because the epidemic was nearer in time to our era, and because the effects were less drastic overall.
Dutch elm disease is caused by either of two species of fungus, Ophiostoma ulmi and Ophiostoma novo-ulmi. These fungi are members of the Plectomycetes series, and are distinguished by having cleistothecia, which is to say ascospores enclosed in a 'sac'. The Ophiostoma fungi are very yeast like in form. Toxins produced by the fungus are carried up conductive vessels, where they cause leaf wilt. The fungal mycelia also block the conducting elements, causing the wood to die. These fungi are spread by bark beetles, usually the native Hylurgopinus rufipes, or the European Scolytus multistriatus beetle. Both beetles, as larvae, chew galleries just below the bark in the outermost annual ring. Each gallery has a main chamber from which radiates a series of blind tunnels. The eggs were laid in the main chamber, and the individual larvae each chew out one of the side tunnels. The Ophiostoma fungi use the beetles as vectors, the spores growing on the inside of the tunnels rub off on the larvae, and more importantly they brush onto the adults that emerge from the pupae. Apparently spores can also be eaten by the beetles, and survive passage through their digestive tracts. The pupated adults then fly off, bearing spores which may infect the elm on which the beetles lay their eggs. The fungi are introduced to a new elm when the beetle lays its eggs in the bark of a new tree. The fungi then attack the sapwood of that new elm.
Since elms only have a few actively conducting annual rings, the fungi in this thin sapwood have a greater impact than they would if the sapwood layers were thicker. The fungal mycelia do not remain confined to the vicinity of the larval galleries. The fungus spread throughout the sapwood, including the conductive wood of the roots. Sometimes the mycelia can cross from the roots of one elm to another. Elms often have their roots fused with neighbouring elms.
Elms infested with the 'Dutch elm disease' may die in the same year as they are infected. Often they die slowly over the span of a few years. Older trees are more likely to be infected than young ones.
Most elms, except for a few Asian species, are sensitive to the Dutch elm disease fungus. However, the largest native elm, the American elm or white elm (Ulmus americana), is very susceptible to Dutch elm disease.
Dutch elm disease originated in Asia, spread to Europe and then to North America. Probably the disease arrived on a shipment of lumber. It made its first appearance in Ohio in 1930. By the 1950s thousands of white elms were dying throughout North America. By 1970 most truly large elms were dead giant hulks with slabs of bark peeling off. The disease seems to have flared up again in the 1990s, as some of the small surviving elms grew to medium size, and then caught the disease.
White elm did not go into a sharp decline, rather it was that old well formed trees became increasingly uncommon. Many white elm saplings live long enough to produce a seed crop before they are killed by the fungus. Some of the Asian elms are less susceptible, including Siberian elm which is a popular city tree. There are several wild species of elm also, each with varying ability to withstand the fungus. There are, in short, plenty of wild and domestic elms on which the fungus can perpetuate itself. The fungus is not 'burning itself out'. Nevertheless, the white elm could be taking the long slow route to extinction.
Several people, including Bernd Heinrich of the University of Vermont, have suggested that white elm could survive Dutch elm disease. It has been noted that some elms develop seed earlier than others. This is due to ordinary genetic variation. Since Dutch elm disease afflicts older trees more often than young ones, there is therefore natural selection for white elms that flower at a younger age. Perhaps, white elm is evolving from a tree into a large shrub.
Control
There have been attempts to find resistant strains of white elm. There are systemic fungicide injections that can control the fungus. These must be repeated every year or so, and they are fairly expensive. New methods aim, instead, to stimulate and enhance the natural defences of the elm trees. The process is like 'inoculation'. Although, the 'immune system' of plants is much simpler than the immune system of animals. Plants do build-up chemical defences to irritants. Thus, one can 'trick' the plant into mounting a defensive response, with a chemical stimulus. Since the defences build up in the absence of an actual fungal attack, the elm becomes pre-prepared for a real fungus infestation.
If there are many elms to treat, systemic fungicides and inoculants may be an impractical solution to the problem. In practice, this means that white elms usually die, and must be removed by a qualified arborist. The cost of removal may exceed $1600.00 cdn, if the elm is large.
References
Eastman, John. 1992. The Book of Forest and Thicket. Stackpole Books. Mechanicsburg, PA.
Holliday, Paul. 1989. A Dictionary of Plant Pathology. Cambridge University Press. Cambridge.
Heinrich, Bernd. 1997. The Trees of My forest. Cliff Street Books. New York. 49-58.
Ware, George H. 1995. Little-known elms from China: landscape tree possibilities. Journal of Arboriculture. 21(6): 284-288.
Butternut Canker
In 1991 a canker disease was noticed in butternuts (Juglans cinerea). Within a few years it was to be found decimating butternuts, a tree that was never common to begin with. It is believed that the fungus is an introduced species. Though, this is not certain.
The wilt is caused by fungus called Sirococcus clavigignenti-juglandacearum. Like most canker fungi it causes wounds that heal slowly, if at all. It also causes a tell-tale slime-flux or gummosis. And like too many fungal diseases it cannot be easily eradicated once a tree is infected. Luckily, some strains and hybrids are fairly resistant to the fungus.
The situation has gotten serious enough that in Ontario butternuts are on the Endangered Species List. Though, many states in the USA have not taken this step – yet. If you suspect butternut canker in your neighbourhood, call the nearest Urban Forestry Service, or a professional arborist. They can help with diagnosis and suggestions for further action.
References
Holliday, Paul. 1989. A Dictionary of Plant Pathology. Cambridge University Press. Cambridge.
Kerr, Pat. 2008. Keeping the historic Butternut alive in Canada. Tree Service Canada. 2(1): 15.
Ross-Davis, A., Huang, Z. McKenna, J., Ostry, M. and Woeste, K. 2008. Morphological and molecular methods to identify butternut (Juglans cinerea) and butternut hybrids: relevance to butternut conservation. Tree Physiology. 28: 1127-1133.
Pine Diplodia
'Diplodia' is now the common name for the Shaeropsis sapinea fungus. 'Diplodia' is the former generic name of the Shaeropsis sapinea fungus. The Diplodia genus still exists, but is occupied by other closely related fungi. Shaeropsis sapinea is a Coelomycetes fungus. It is best known for its infestations of firs and pines, in particular the Austrian pine ( Pinus nigra ). Austrian pine is a European species that is now a common urban tree in North America.
Symptoms of diplodia infestations begin with a yellowing of the new tip leaves (needles) of a pine. By the summer and autumn of the year of yellowing, leaves fall in great masses. (Diplodia is sometimes considered a 'needle cast' fungus.) If a branch becomes denuded of leaves, the whole branch dies. Often lower branches show these symptoms first, and then they spread to the upper crown. Although, this sequence does not always follow. In Austrian pine infestations of diplodia can defoliate the tree in the second or third year after the onset of symptoms. Before this, several branches in the mid crown may be dead or dying.
Unfortunately, Austrian pines have in the past often been planted together in large numbers. Residential and industrial sites may have virtual forests of such pines. It is not uncommon for several trees to develop diplodia in one year and spread the disease to others the next. Consequently, with a span of two years, dead and dying pines are scattered all over the property. Tree removal professionals may like the results of diplodia, but property managers generally do not.
Go to: Other needle cast fungi.
Control
Although, in theory it is possible to stay the effects of the fungus with injection of fungicides, in practice this is seldom done. For even if successful, the fungus has probably spread to other trees, and almost certainly large portions of the crown have been disfigured already . Old Austrian pines tend to be more often afflicted than the young. Indeed, diplodia very often kills Austrian pines which are near the end of their life cycle.
Austrian Pine
Austrian pine, Corsican pine or black pine (Pinus nigra) is a sturdy pine. The leaves occur in bundles of two, they are dark, long, stiff and bristle tipped. The crown of a healthy Austrian pine is very thickly foliated. The cones are large and rounded. The pine can grow up to 30 metres tall. Austrian pine occurs in nature in the southern Apennine, and the Mediterranean highlands in Greece, Corsica and Sicily.
Austrian pines are not long lived, nor are they hardy in most of North America. American seasons are generally more extreme in temperature, and drought stress, than are the seasons in Europe. Quite often, in fact, drought stress, root compaction, and other physical stresses, precede the onset of diplodia infection. Thus, ‘stress’ is said to make the pines more susceptible to disease in general. This ‘stress’ explanation has become a cliché, some scepticism is called for. Watering and fertilising, although generally good for a tree, probably will not much improve the chance of survival for diplodia infected Austrian pine.
Austrian pines were once a favoured urban tree species, because they are cheap and fast growing. Their short life span, and susceptibility to diplodia make them a poor urban tree choice. They also have very large cones, which are a hassle for groundskeepers and lawn mowers. Cost considerations often tempt developers and property buyers to choose plant Austrian pines as ornamental trees for residential and industrial sites. My recommendation is: do not plant Austrian pine .
References
Holliday, Paul. 1992. A Dictionary of Plant Pathology. Cambridge University Press. Cambridge. 92, 302.
Witches's Brooms
Witches' brooms are clusters of stunted, closely packed distorted twigs growing on trees or shrubs. From a distance the tangled mass of a witch broom may look like a mistletoe, squirrel's nest or a bird's nest. Usually these deformities are confined to a small region on a plant. Witch broom deformities are instigated by several different agents, viral, phytoplasmal and fungal. In all cases the infectious agent apparently distorts the normal growth pattern of the plants. The growth tends to follow the same architectural programme as normal tissue, but the rates of growth, the ultimate size and the symmetry of the plant are disrupted.
Taphrina spp. are Ascomycete fungi that can cause witches' brooms on birch (Betula spp.), plum (Prunus spp.) and hornbeam (Carpinus spp.). Different Taphrina species afflict different host plants. Those Taphrina species that do not cause witch broom distortions usually cause leaf, flower or fruit distortions. Some Taphrina species cause leaf curl diseases, leaves that are cup-shaped and not flat. Others cause twisted asymmetrical fruit, as manifest in the pocket plum disease.
Melampsorella caryophyllacearum is a 'rust' or Uredinales fungus. It can cause cankers or witch broom deformities on fir trees (Abies spp.). Like many rust fungi, the 'fir rust' has alternate hosts. Fir rust can infect chickweed (Cerastium) and stitchwort (Stellaria). Like other rust fungi, different kinds of spores, sexual and asexual, occur on the different hosts. The aeciospores produced on the fir originate from the union of 'male' spermatia and 'female' receptive hyphae.
Phytoplasmas are another agent that can cause witches' brooms to develop on locust (Robina spp.) and apple (Malus spp.). Phytoplasmas are tiny monera similar to bacteria.
Control
There is little evidence that witches' brooms cause any serious harm to a tree. However, they are sometimes considered unsightly. If one insists on removing witches' brooms, pruning off the offending broom is an effective treatment. Winter is the best time for removing witches' brooms. It is recommended that witches' brooms be burnt after they are removed.
Bedeguar Galls
Sometimes around mid-summer one can find strange mossy growths on roses (Rosa spp.). These look like tiny deformed tendrils all bunched up in a mass of several centimetres width. Usually they are pallid green, with strands of red and yellow. These are ‘bedeguar’ galls.
Bedeguar galls are galls instigated by wasps (Diplolepis rosae). The tiny female wasps lay their eggs inside young buds. The growing buds form the deformed bedeguar growths. The larvae dwell within little chambers at the centres of these growths. The adults do not emerge from these galls until the following spring.
Bedeguar galls, once established, can only be controlled by pruning them off. Luckily, they do not afflict trees in the rose family.
References
Buszacki, Stefan and Harris, Keith. 1998. Pest, Diseases & Disorders of Garden Plants. Harper Collins Publishers. London. 338, 383-393, 451-454.
Viroids, Viruses and Phytoplasmas
Graft-Transmissible Agents
Plants are often infected with viruses and viroids. Many of these viruses have been specifically identified. For others, their existence has been surmised on the basis of virus-like symptoms. When no identified virus or bacterium has been verified, botanists often call the disease a 'graft-transmissible agent'. The term refer to the fact that the agent can be transmitted by grafting, or contact between plants, just like a virus. It is suspected that some graft-transmissible agents are viroids.
Mosaic Viruses
A virus is an micro-organism that exists as a complete cellular parasite. A virus utilises the cellular mechanisms of their host for their replication. They have either DNA or RNA based gene sequences that are 'read' by the host cell. The host cell is 'tricked' into replicating the virus' genome and its proteins. Viruses are capable of very limited self-activated responses, such as penetrating the host cell membrane.
Viruses and graft-transmissible agents generally either cause deformed growth, or mottling of leaves. Deformities may include stunted growth, or misshapen roots, stems, leaves, flowers or fruit. Leaf mottling is an especially common symptom of virus infection. Each 'mottle' being a location where virus replication causes either tissue necrosis or interruption in cell function. If the mottling is tight it forms a 'mosaic' pattern, hence the term mosaic virus.
There are ‘viruses’ with some of their own functional genes. These are the Mimiviridae which include the Mimivirus. These weird creatures are hundreds of times more massive than most ‘normal’ viruses. The mimiviruses are built like small bacteria. They are parasites mostly of protozoa and animals.
Viroids
Viroids are basically viruses that lack a protein coat. Many viroids have been identified, the genomes of several have even been mapped. Viroids consist only of strands of RNA. Viroids have the shortest and simplest known genetic sequences of any 'living' thing. One viroid, the potato spindle tuber virus (PSTV) that infects potatoes, has only 359 nucleotide bases in its genome! A viroid that infests oranges, citrus exocortis (CEV), has only 371 nucleotide bases. Like viruses, viroids are complete cellular parasites, they require living cells to replicate their genes for them.
References
Grierson, D. and Covey, S.N. 1988. Plant Molecular Biology. 2nd Edition. Blackie. London. 178-181.
Phytoplasmas - MLOs
Some graft-transmissible agents which were originally thought to be viroids or viruses have actually been identified as phytoplasmas. Phytoplasmas are basically very tiny Gram Positive bacteria in the Class Mollicutes. They are similar to the mycoplasmas that cause a number of diseases in animals. Phytoplasmas were once commonly known as “mycoplasma like organisms” (MLOs). Phytoplasmas lack cell walls, but they do have cell membranes and an active metabolism. Their nucleotide sequences have several thousand base pairs. They are obligate parasites in that they lack the ability to live without their hosts. Consequently, they have reduced amounts of DNA and proteins within them. Phytoplasmas are quite small, only a few hundred nanometres wide (70-1000 nm). This is just larger than the enigmatic nanobacteria.
Phytoplasmas are known to cause a number of diseases in plants. They live inside their host cells' cytoplasm. Many MLOs can be spread from plant to plant via sap-feeding insects. Symptoms of phytoplasmic disease often involve disturbances in the growth of plant tissues. For example, apple chat phytoplasma causes apples to cease development before they rippen properly. Apple proliferation phytoplasma causes 'witches brooms', a tangle of distorted twigs and leaves. Apple rubbery wood phytoplasma causes flexible rubbery shoots. These are just a few examples that infest apples. Others phytoplasma diseases infect roses, strawberries, and various garden vegetables. Some very important forest diseases are MLOs. Elm yellows and ash yellows are caused by phytoplasmas.
There are presently no effective cures for phytoplasma diseases. The spread of these bacters can be controlled by removing and burning infected twigs. Avoid any sort of contact between the infected plant tissues and healthy plants.
Black Knot
Black knot (Apiosporina morbosa) is a fungus that attacks the cherries, plums, apricots, almonds and other species in the genus Prunus. (An old name for the fungus was: Dibotyron morbosum). Infections start in wounds in the bark. Usually the visible symptoms are manifest the following year. Hard black rough growths swell up around the wound and expand into sausage shaped masses. The 'knots' can both grow and spread into uninfected twigs. In the spring olive-green spores form on the knots.
Control
If the fungal knots start on large stems, or spread to them, the damage may become difficult to rectify. Knot - cankers on trunks can kill the tree. The best method of control is to prune off the infected twigs several centimetres back from the knot. These cuttings mst be disposed of, ideally they should be burnt. At any rate, pruning tools must be sterilised before being used on other trees.
Damping-Off
Damping-off is a catch-all term for soil fungoids which cause butt-rot in seedlings. Oomycetes in the Pythium genus are a widespread cause of this rot. The damping-off fungoid usually waits dormant in the soil in spore form, ‘hatching’ only when a suitable host plant becomes available. Damping-off infection is visible as a blackening of bark near the root crown. If the rot is extensive enough, the seedling may die. Usually humid environments favour the damping-off infestation. The disease is a problem mostly, but not exclusively, in greenhouses. In an urban forestry context, it is mostly a problem for the tree-nursery, not the homeowner.
Control: One can sterilise the greenhouse compost, with heat or fumigants, before seeding. Ultimately, soil should not be too vigorously sterilised, as beneficial mycorrhizae could be killed in the process. In general, damping-off can be minimised by good soil hygiene, and by not allowing the seeding milieu to become too damp.
Mildews & Moulds
‘Mildew’ is a catch-all term for organisms which cause mouldy rots. Mildews, as a whole, are somewhat more common in moist shaded areas than in dry areas with bright sunlight. Pathogenic mildews are not easily distinguished from pathogenic moulds (U.S. spelling: ‘mold’). The term ‘mildew’, to a plant pathologist, signifies the parasitic downy and powdery mildews.
| Phylum | Spores |
| Ascomycota Sac Fungi |
 |
| Basidiomycota Club Fungi |
|
| Deuteromycota Fungi Imperfecti |
|
| Oomycota Water Mould |
|
Biofilms
Various kinds of bacteria, slime mould amoebae, yeast fungi and even algae can form ‘scums’ on plant surfaces. The slime of these biofilms can be composed of a gelatinous matrix of water, polysaccharides and proteins. The organisms excrete the gelatine to protect their little microbial community. Sometimes the slimes are composed of several species. Some of the species may be mutualistic, others may be predatory.
Biofilms on plants are usually not pathogenic in themselves. Generally, they are merely symptomatic of an extremely humid milieu. They can, however, be precursors to true mould infections.
Downy Mildew
Downy mildews are oomycete fungoids in the Peronospraceae family. The branched sporangia are large enough to appear, to the unaided-eye, as downy or cottony masses. These obligate parasites feed on a wide range of plant tissues. Most species are very host specific. They are not as likely to be a major landscape problem as are the powdery mildews.
Control: Oomycetes are not easily controlled by copper fungicides. (They are not fungi.) Mancozeb is somewhat effective in killing the fungoid.
Powdery Mildew
Powdery mildews are ascomycete fungi in the Erysiphaceae family. The masses of mycelium on plant tissues may look to the human eye like a fine white to grey powder. Generally the fruiting-bodies are smaller than those of the downy mildews. The fine mycelia feed on plant cells, weakening them in an overall general sense. Distortions of growth may occur if young growing tissues are infected.
Control: Sulphur based fungicides can inhibit the growth of powdery mildew. However, several applications during dry weather are usually necessary. Synthetic fungicides are more effective and require fewer treatments.
Fungi Imperfecti
The Deuteromycota, or Fungi Imperfecti, are those fungi which originally were not assignable to specific taxonomic groups. They could not be assigned because they had no distinguishing visible features that could identify them as either basidomycetes, ascomycetes or other fungal taxa. Increasingly, genetic studies have identified the taxonomic affinities of the imperfect fungi. For example, the so-called 'Botrytis cinerea' mould is actually a race of the ascomycete Botryotina fuckeliana. The grey mould form does not produce ascospores. The Botryotina fuckeliana form does produce such spores. The Monilia brunnea fungus which lives symbiotically with ambrosia beetles was an imperfect fungi. Its genetic affiliation links it to the ascomycetes. Ascomycetes are somewhat more prone to being imperfect fungi than are the basidiomycetes. Those imperfect fungi which seem to lack even a conidial phase are called mycelia sterilia (i.e. sterile mould). Due to the vast numbers of imperfect fungi species, the reclassification process is still incomplete.
Sooty Mould (Mold)
Sooty moulds are an assorted set of saprobic fungi. They appear as dark mouldy patches on leaves, twigs or stems. These fungi are not directly disease agents. They feed off the faeces of aphids, and other insects with sugary excretions. The insects, not the fungi, are more likely to be the actual health problem.
Control: Sooty moulds are usually confined to regions of the plant with sap feeding insects on them. If sap-feeders are identified as the culprits, the insects need to be controlled, not the fungi.
Grey Mould - Gray Mold
Grey mould (gray mold) is a fungus that consist of mycelium strands growing on and within plant tissues. In moist conditions the fungus can begin to grow on leaves, twigs and fruits. Basically, it causes soft tissues to rot. 'Grey mould' is a general name. Many different fungal species have been labelled 'grey moulds'. The pseudo-generic name Botrytis has been given to many of the Fungi Imperfecti that cause grey mould.
Control: Sulphur based fungicides can kill grey mould, if applied in time. Increasing ventilation so as to dry the plants also helps check the spread of the fungus. Drying is not always practical for outdoor plants. The best advice is to trim off dead branch stubs, as the fungal attack often starts in dead tissues.
References
Buszacki, Stefan and Harris, Keith. 1998. Pest, Diseases & Disorders of Garden Plants. Harper Collins Publishers. London. 547-588.
Harrison, J.J., Turner, R.J., Marques, L.L.R. and Ceri, H. 2005. Biofilms. American Scientist. 93 (6): 508-515.
Holliday, Paul. 1992. A Dictionary of Plant Pathology. Cambridge University Press. Cambridge. 92, 302.